Interaction of calcium and cyclooxygenase inhibitors on transport by the turtle and toad bladders.

Agents or maneuvers which increase intracellular calcium, inhibit Na, H + and AVP-stimulated water transport by the turtle and toad bladders. The mechanism of the inhibitory effect remains incompletely defined. An increase in intracellular calcium has been shown to stimulate prostaglandin release in several tissues. Since prostaglandins are capable of altering transport we examined whether cyclooxygenase inhibition would alter the inhibitory effect of the high extracellular calcium, ionophore A23187, or carbachol on AVP-stimulated water flow in the toad bladder and on Na and H + transport measured as the short circuit current and reverse short circuit current respectively by the turtle bladder. Indomethacin or ibuprofen was used at a dose of 10(-6) M which has been shown to inhibit the release of endogenous prostaglandin. Pretreatment with indomethacin or with ibuprofen significantly decreased the inhibitory effect of high extracellular calcium, ionophore, or carbachol on AVP-stimulated water flow in the toad bladder. Pretreatment with indomethacin did not alter the inhibitory effect of the ionophore or carbachol on Na or H + transport by the turtle bladder. The data demonstrate that pretreatment with indomethacin or ibuprofen blunts the effect of agents which increase intracellular calcium on water transport but not on Na or H + transport. It is suggested that high intracellular calcium inhibits water transport via prostaglandin release whereas the inhibition of Na or H + transport is independent of prostaglandin.